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首页> 外文期刊>Cell cycle >Fos-dependent induction of Chk1 protects osteoblasts from replication stress
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Fos-dependent induction of Chk1 protects osteoblasts from replication stress

机译：Fos依赖的Chk1诱导保护成骨细胞免受复制压力

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摘要

Stable Fos expression in the osteoblast lineage results in the development of steosarcomas (OS) in mice, yet the underlying mechanisms are poorly understood. Using a genetic system in which Fos expression can be induced in osteoblasts in a doxycycline-dependent manner and through subsequent RNA sequencing and gene set enrichment analysis, we were able to identify novel transcriptional targets of Fos in osteoblasts. These included a distinct activation of cellular response toward replication stress (RS), exemplified by a Fos-dependent induction of the RS-suppressing Chk1 kinase. Importantly, Fos expression protects osteoblasts from RS and DNA damage likely through upregulation of Chk1 and facilitates transformation by Ras/E1A oncogenes. These data reveal a novel function of Fos in safeguarding genome stability during replication, which is particularly relevant in conditions of oncogene-induced S-phase entry.
机译：成骨细胞谱系中稳定的Fos表达导致小鼠肉瘤（OS）的发展，但其潜在机制了解甚少。使用可以以强力霉素依赖性方式在成骨细胞中诱导Fos表达的遗传系统，并通过随后的RNA测序和基因集富集分析，我们能够鉴定成骨细胞中Fos的新转录靶点。这些包括细胞对复制应激（RS）的独特激活，例如RS抑制Chk1激酶的Fos依赖性诱导。重要的是，Fos表达可保护成骨细胞免受可能通过Chk1上调引起的RS和DNA损伤，并促进Ras / E1A癌基因的转化。这些数据揭示了Fos在复制过程中维护基因组稳定性的新功能，这在致癌基因诱导的S期进入条件下尤其重要。

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